 Hey everybody, I'm from the University of Tennessee, Memphis, Tennessee, originally from Oak Ridge, which is near Knoxville. So this was a 68-year-old Caucasian male with a history of primary opening with glaucoma and field filtration surgery in the left eye, who presented to the Emergency Department on postoperative day five from an Ahmed glaucoma valve in the left eye and presented with acute vision loss and pain in that eye. His past medical history was significant for diabetes, hypertension, hyperlipidemia, a remote history of a meningioma. He had an ocular history of primary opening glaucoma and cataracts in both eyes, as well as a surgical history of trabeculectomies and cataract extraction in both eyes. His medications listed in his review of systems was negative for fever or chills. So on exam, he had a visual acuity of 2050 in the right and light perception in the left eye. His pupils were 3 to 2 millimeters in the right and 3.5 millimeters and minimally reactive with a positive APD in his left eye. His pressures were 10 in the right and 2 in the left. Lids, lacrimal, and lashes were within normal limits. The conjectiva and sclera showed flat and vascularized blood superiorly in both eyes, as well as a well-covered Ahmed glaucoma valve in the left. His conjectiva was clear in the right, and he had iris stochornia touch in the periphery of the left eye. The anterior chamber of the right eye was deep and quiet. The left eye was shallow and again showed iris stochornia touch, but no lens stochornia touch. And there was the tube from the valve was plugged by forward iris, and there was a 25 percent hyphaema. Both irises had superior peripheral iridotomies, and his lenses were posterior chamber IOLs in both eyes, and there was no view to the back on the left. So before I continue, what would be your differential diagnosis? Okay, so this is a differential diagnosis just for a flat anterior chamber, and in our patient, he had a low intracular pressure, but for the sake of the differential, someone presenting like this with high intracular pressure, you would first want to see if there was a pupillary block. If there was, consider acute angle closure. No pupillary block could be aqueous misdirection syndrome, and then a postoperative patient, supercruital hemorrhage. So low intracular pressure could be over filtration or a blob leak, probably most commonly in this type of postoperative patient. It could also be aqueous suppression, acute chorodal effusion, or amniolary ciliary body detachment. So this is the image from the night he presented, and you can see a dome-shaped elevation, which is echolucent behind it, and there actually was an oppositional dome-shaped elevation. You can't really see it from this picture, but it was present. So he had a chorodal effusion, so chorodal detachment is a few complication of intracular surgery, and it's the most common posterior segment complication of aqueous drainage surgery, and it's generally attributable to postoperative hypotony. So some other causes, not surgically related, are eye trauma, corneal ulcers, PRP, and the use of IOP lowering medications. If it occurs idiopathically, it can be termed uveal effusion syndrome, which happens in healthy middle-aged males, pretty typically, and majority are bilateral. If chorodal detachment occurs without any evidence of intracular surgery or trauma, you would want to investigate neoplastic vascular inflammatory causes. So chorodal detachment can either be serious or hemorrhagic, and they present somewhat differently. So serous effusions can be asymptomatic or painless if they're small or peripheral. Larger effusions can cause a myopic shift because of the anterior displacement of the lens. There may be a reduction in visual acuity depending on its location and the proximity to the visual axis, and there may be a scatoma at the side of the fusion. Super chorodal hemorrhage characteristically presents sudden throbbing pain in the eye, headache, nausea, vomiting, marked infection, and visual acuity. And the visual outcome and overall prognosis is worse than a serous effusion. So if you were able to see the back, you can appreciate there's a dome-shaped elevation with transillumination and fixed adherence to the vortex veins, and then super chorodal hemorrhage would look similar without the transillumination because of the blood. And then on B-scan, similarly, you see a dome-shaped elevation, and this is a picture of a chorodal effusion, so there's echolucent behind it. And there's an hourglass configuration because of the firm attachments to the vortex veins. And then retinal detachments look different on B-scan because they are mobile, whereas both types of chorodal detachment are immobile. So some of the pathogenesis of chorodal detachment is just an accumulation of serum or blood in the potential space between the chloride and the sclera. Postoperatively, the most common cause is hypotony. And hypotony, leading to serous effusion, can be further exacerbated by the reduction in aqueous humor production if there's an annulary ciliary body detachment or if there's inflammation, those can further reduce aqueous humor production. And then serous effusion is thought to be caused by a pressure gradient that can occur in one of three ways. So hypotony, which is decreased extravascular pressure, increased venous pressure, so the increased capillary wall pressure, or ocular inflammation, which causes vascular permeability. And then supercordal hemorrhage is thought to be caused by a rupture of the posterior ciliary arteries following cordal effusion. And this is just a schematic of the three causes. So hypotony, decreased interstitial pressure, and then you have pressure from the capillaries into the interstitium. Increased capillary pressure produces a similar effusion and then inflammation causing vascular permeability. So this is just a list of predisposing factors. And then in our patient, the factors are highlighted. So any type of systemic disease that injures the vessels is a predisposing factor, glaucoma, and then probably the biggest factor for him was his recent intraocular surgery. So some of the morbidities, lens opacities, occur in a significant proportion of patients who have cordal detachment. Corneal endothelial damage can occur, especially if there's iris to cornea touch or lens to cornea touch. Peripheral anterior, sneaky eye, maculopathy, and globes thesis. But interestingly, one study found that the success of the trabeculectomy wasn't affected by the cordal detachment. And then supracordal hemorrhage is associated with the worst prognosis, and the prognosis really depends on the time point that the supracordal hemorrhage occurs. So expulsive or intraoperative supracordal hemorrhage is associated with the worst visual prognosis than delayed supracordal hemorrhage. So preventative measures, obviously, if the patient has hypertension or glaucoma, pressure and intraocular pressure control prior to surgery, discontinuation of anticoagulants and anti-platelets if possible. And then intraoperatively, when patients undergoing trabeculectomy, there is a higher incidence of cordal detachment with the use of antifibrotics. So in patients with a lower risk of scarring, so primary trabeculectomy, if they have a thin conjectiva or the elderly, consider no antifibrotics or 5FU only. But in patients who have a higher risk of scarring, mydomycin C is indicated. So the majority of patients can be treated medically and followed with topical corticosteroids and cycloplegics to posteriorly shift that lensiris diaphragm. But there are indications for surgical intervention, and these are the indications for supracordal hemorrhage. So intractable pain, displacement of the vitreous into the anterior chamber, and carceration of the vitreous into the wound, and coexisting with vitreous hemorrhage. And ideally, if you're performing surgery on a supracordal hemorrhage, you would want to wait to allow the clot to liquefy prior to draining, and you can follow this either with B scan or it's thought that waiting 7 to 10 days is enough time for this to happen. But if the intracular pressure is severely elevated, you may need to perform surgery immediately to relieve the compartment syndrome that's developing and prevent ischemic damage. And then these are the indications for caroidal effusion surgical intervention. So retinal damage, oppositional caroidal effusions or kissing caroidals, which we had in our patient. So obviously you would want to intervene to prevent vitreous adhesions and eventual retinal detachments. A flat anterior chamber that leads to corneal damage. So if there's evidence of lens cornea touch or iris cornea touch as we had or endothelial corneal damage and acceleration of lens opacities or the evidence of marked intracular inflammation. And finally the last indication is just persistent caroidal detachment that fails to resolve. So surgical treatment, the first option which can be performed at the slit lamp is just anterior chamber reformation to kind of reverse the hypotenuse. So using the paracentesis and the injection of viscoelastic into the anterior chamber. Posterior sclerotomy also may be performed so similarly pressurizing the anterior chamber and then using the B scan to determine which quadrants have the largest effusions, incisions are made and full thickness circumferential incisions are made 2 millimeters long. The trectomy may be indicated for massive supercordal hemorrhage or supercordal hemorrhage with vitreous incarceration into the wound. And this is just an image and this is a video. So the scleral flap has been made and the incision has been made and you can just see the serous fluid draining from the wound. So back to our patient. Upon further questioning he admitted to straining earlier that day so could have contributed to his acute effusion. And he was taken back that night for posterior sclerotomies in the left eye and serous fluid was drained from the wounds. On postoperative day one this is his B scan so he still had oppositional cordial effusions. He was started on Vigamox, continued on Predforte, he had a pressure of six and was still light perception. On postoperative day three he was still light perception, still had some opposition. So on postoperative day nine he was taken back for repeat drainage from the same sclerotomy sites. He had an intracular pressure of ten after injection of Helan into the anterior chamber and his visual acuity improved to 2400 and you can see some distance now. On postop day 15 he was light perception and his B scan looked worse so Helan GV was injected into the anterior chamber and his pressure was brought from 8 to 20. And then postop day 17 his intracular pressure improved to 15, visual acuity improved to 2200, was continued on Cycloplegia and this is from day 17 here. And then postop day 24 his visual acuity improved to 2080. Any questions? I think the last time I heard was the 2080 vision but he's continuing to follow up, it was like a little over a month ago. It wasn't this patient, it was a different patient. There wasn't a video of this patient.